ArticleMolecular and cellular biology2000
Evi9 encodes a novel zinc finger protein that physically interacts with BCL6, a known human B-cell proto-oncogene product.
Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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59 citing papers in PubMed, 100 citations in OpenAlex.
- The BCL11A transcription factor stimulates the enzymatic activities of the OGG1 DNA glycosylase.Biological chemistry · 2024Article
- Repression of developmental transcription factor networks triggers aging-associated gene expression in human glial progenitor cells.Nature communications · 2024Article
- Review
- Transcriptional Repressor BCL11A in Erythroid Cells.Advances in experimental medicine and biology · 2024Review
- A feedback loop between lncRNA MALAT1 and DNMT1 promotes triple-negative breast cancer stemness and tumorigenesis.Cancer biology & therapy · 2023Article
- miR-365-3p mediates BCL11A and SOX6 erythroid-specific coregulation: A new player in HbF activation.Molecular therapy. Nucleic acids · 2023Article
- Deciphering clinical significance of BCL11A isoforms and protein expression roles in triple-negative breast cancer subtype.Journal of cancer research and clinical oncology · 2023Article
- RNA-seq analysis reveals candidate genes associated with proliferation, invasion, and migration in BCL11A knockdown B-NHL cell lines.Annals of hematology · 2023Article
- BCL11A Expression in Non-Small Cell Lung Cancers.International journal of molecular sciences · 2023Article
- BCL11A Expression in Breast Cancer.Current issues in molecular biology · 2023Article
- The DNA repair function of BCL11A suppresses senescence and promotes continued proliferation of triple-negative breast cancer cells.NAR cancer · 2022Article
- Developmental cell death of cortical projection neurons is controlled by a Bcl11a/Bcl6-dependent pathway.EMBO reports · 2022Article
- BCL11A promotes myeloid leukemogenesis by repressing PU.1 target genes.Blood advances · 2022Article
- A novelFrontiers in molecular neuroscience · 2022Article
- Molecular analysis of the erythroid phenotype of a patient with BCL11A haploinsufficiency.Blood advances · 2021Article
- Bcl11 Transcription Factors Regulate Cortical Development and Function.Frontiers in molecular neuroscience · 2020Review
- MicroRNA-146a Is a Wide-Reaching Neuroinflammatory Regulator and Potential Treatment Target in Neurological Diseases.Frontiers in molecular neuroscience · 2020Article
- BCL11A Promotes the Progression of Laryngeal Squamous Cell Carcinoma.Frontiers in oncology · 2020Article
- BCL11A: a potential diagnostic biomarker and therapeutic target in human diseases.Bioscience reports · 2019Review
- BCL11A rs1427407 Genotypes in Sickle Cell Anemia Patients Undergo to Stroke Problems in Sudan.Korean journal of family medicine · 2019Article
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Evi9 is a common site of retroviral integration in BXH2 murine myeloid leukemias. Here we show that Evi9 encodes a novel zinc finger protein with three tissue-specific isoforms: Evi9a (773 amino acids [aa]) contains two C(2)H(2)-type zinc finger motifs, a proline-rich region, and an acidic domain; Evi9b (486 aa) lacks the first zinc finger motif and part of the proline-rich region; Evi9c (239 aa) lacks all but the first zinc finger motif. Proviral integration sites are located in the first intron of the gene and lead to increased gene expression. Evi9a and Evi9c, but not Evi9b, show transforming activity for NIH 3T3 cells, suggesting that Evi9 is a dominantly acting proto-oncogene. Immunolocalization studies show that Evi9c is restricted to the cytoplasm whereas Evi9a and Evi9b are located in the nucleus, where they form a speckled localization pattern identical to that observed for BCL6, a human B-cell proto-oncogene product. Coimmunoprecipitation and glutathione S-transferase pull-down experiments show that Evi9a and Evi9b, but not Evi9c, physically interact with BCL6, while deletion mutagenesis localized the interaction domains in or near the second zinc finger and POZ domains of Evi9 and BCL6, respectively. These results suggest that Evi9 is a leukemia disease gene that functions, in part, through its interaction with BCL6.
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